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Recent Progress in Multiple Sclerosis
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Recent Progress in Multiple Sclerosis

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Biochemistry".

Deadline for manuscript submissions: closed (30 November 2021) | Viewed by 19637

Special Issue Editors

Prof. Dr. Arnon Karni

E-Mail Website
Guest Editor
Department of Neurology, Tel Aviv Sourasky Medical Center, Tel Aviv-Yafo 6423906, Israel
Interests: multiple sclerosis
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Friedemann Paul

E-Mail Website
Guest Editor
Clinical and Experimental Multiple Sclerosis Research Center, Charité—Universitätsmedizin Berlin, D-10117 Berlin, Germany
Interests: multiple sclerosis and neuromyelitis optica; neuroimaging; retinal optical coherence tomography; neuroprotection; dietary modulation of neuroinflammation
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Multiple sclerosis is the most common disease that leads to neurological disability in young people. Despite the advances over the years in understanding the disease, more knowledge is needed about the specific mechanisms of the relapses versus progression independent of relapses, the immediate damage caused by the formation of a new lesion and the secondary damage induced over time due to the demyelination and axonal damage. Inflammatory activity is, on the one hand, harmful but may also be protective. The various approaches to inducing the repair of the damage caused and the development of various imaging and molecular paraclinical biomarkers that demonstrate different aspects of disease activity and progression and the degree of response to treatment are worthy of study. All of these and more represent a broad and intensive field of research that will expand our understanding of the disease and lead to exciting discoveries.

The objective of this Special Issue, “Recent Progress in Multiple Sclerosis”, is to describe and bring together the most recent research conducted in the fields of the pathophysiology, of various biomarkers, and the treatment and repair of multiple sclerosis.

Prof. Dr. Arnon Karni
Prof. Dr. Friedemann Paul
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • multiple sclerosis
  • immune pathophysiology
  • remyelination and repair
  • molecular biomarker
  • imaging
  • disease monitoring
  • modifiable environmental factors
  • neuroprotection

Published Papers (6 papers)

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Research

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17 pages, 2721 KiB  
Communication
Siponimod Modulates the Reaction of Microglial Cells to Pro-Inflammatory Stimulation
by Joel Gruchot, Ferdinand Lein, Isabel Lewen, Laura Reiche, Vivien Weyers, Patrick Petzsch, Peter Göttle, Karl Köhrer, Hans-Peter Hartung, Patrick Küry and David Kremer
Int. J. Mol. Sci. 2022, 23(21), 13278; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms232113278 - 31 Oct 2022
Cited by 3 | Viewed by 1714
Abstract
Siponimod (Mayzent®), a sphingosine 1-phosphate receptor (S1PR) modulator which prevents lymphocyte egress from lymphoid tissues, is approved for the treatment of relapsing-remitting and active secondary progressive multiple sclerosis. It can cross the blood–brain barrier (BBB) and selectively binds to S1PR1 and [...] Read more.
Siponimod (Mayzent®), a sphingosine 1-phosphate receptor (S1PR) modulator which prevents lymphocyte egress from lymphoid tissues, is approved for the treatment of relapsing-remitting and active secondary progressive multiple sclerosis. It can cross the blood–brain barrier (BBB) and selectively binds to S1PR1 and S1PR5 expressed by several cell populations of the central nervous system (CNS) including microglia. In multiple sclerosis, microglia are a key CNS cell population moving back and forth in a continuum of beneficial and deleterious states. On the one hand, they can contribute to neurorepair by clearing myelin debris, which is a prerequisite for remyelination and neuroprotection. On the other hand, they also participate in autoimmune inflammation and axonal degeneration by producing pro-inflammatory cytokines and molecules. In this study, we demonstrate that siponimod can modulate the microglial reaction to lipopolysaccharide-induced pro-inflammatory activation. Full article
(This article belongs to the Special Issue Recent Progress in Multiple Sclerosis)
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18 pages, 2178 KiB  
Article
Combination of Genomic and Transcriptomic Approaches Highlights Vascular and Circadian Clock Components in Multiple Sclerosis
by Chiara Scapoli, Nicole Ziliotto, Barbara Lunghi, Erica Menegatti, Fabrizio Salvi, Paolo Zamboni, Marcello Baroni, Francesco Mascoli, Francesco Bernardi and Giovanna Marchetti
Int. J. Mol. Sci. 2022, 23(1), 310; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23010310 - 28 Dec 2021
Cited by 9 | Viewed by 3549
Abstract
Aiming at exploring vascular components in multiple sclerosis (MS) with brain outflow disturbance, we combined transcriptome analysis in MS internal jugular vein (IJV) wall with WES in MS families with vertical transmission of disease. Main results were the differential expression in IJV wall [...] Read more.
Aiming at exploring vascular components in multiple sclerosis (MS) with brain outflow disturbance, we combined transcriptome analysis in MS internal jugular vein (IJV) wall with WES in MS families with vertical transmission of disease. Main results were the differential expression in IJV wall of 16 MS-GWAS genes and of seven genes (GRIN2A, GRIN2B, IL20RB, IL26, PER3, PITX2, and PPARGC1A) not previously indicated by GWAS but encoding for proteins functionally interacting with MS candidate gene products. Strikingly, 22/23 genes have been previously associated with vascular or neuronal traits/diseases, nine encoded for transcriptional factors/regulators and six (CAMK2G, GRIN2A, GRIN2B, N1RD1, PER3, PPARGC1A) for circadian entrainment/rhythm components. Among the WES low-frequency (MAF ≤ 0.04) SNPs (n = 7) filtered in the 16 genes, the NR1D1 rs17616365 showed significantly different MAF in the Network for Italian Genomes affected cohort than in the 1000 Genome Project Tuscany samples. This pattern was also detected in five nonintronic variants (GRIN2B rs1805482, PER3 rs2640909, PPARGC1A rs2970847, rs8192678, and rs3755863) in genes coding for functional partners. Overall, the study proposes specific markers and low-frequency variants that might help (i) to understand perturbed biological processes in vascular tissues contributing to MS disease, and (ii) to characterize MS susceptibility genes for functional association with disease-pathways. Full article
(This article belongs to the Special Issue Recent Progress in Multiple Sclerosis)
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16 pages, 2105 KiB  
Article
Neuroprotective Effect of Glatiramer Acetate on Neurofilament Light Chain Leakage and Glutamate Excess in an Animal Model of Multiple Sclerosis
by Rina Aharoni, Raya Eilam, Shaul Lerner, Efrat Shavit-Stein, Amir Dori, Joab Chapman and Ruth Arnon
Int. J. Mol. Sci. 2021, 22(24), 13419; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms222413419 - 14 Dec 2021
Cited by 4 | Viewed by 2175
Abstract
Axonal and neuronal pathologies are a central constituent of multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE), induced by the myelin oligodendrocyte glycoprotein (MOG) 35–55 peptide. In this study, we investigated neurodegenerative manifestations in chronic MOG 35–55 induced EAE and [...] Read more.
Axonal and neuronal pathologies are a central constituent of multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE), induced by the myelin oligodendrocyte glycoprotein (MOG) 35–55 peptide. In this study, we investigated neurodegenerative manifestations in chronic MOG 35–55 induced EAE and the effect of glatiramer acetate (GA) treatment on these manifestations. We report that the neuronal loss seen in this model is not attributed to apoptotic neuronal cell death. In EAE-affected mice, axonal damage prevails from the early disease phase, as revealed by analysis of neurofilament light (NFL) leakage into the sera along the disease duration, as well as by immunohistological examination. Elevation of interstitial glutamate concentrations measured in the cerebrospinal fluid (CSF) implies that glutamate excess plays a role in the damage processes inflicted by this disease. GA applied as a therapeutic regimen to mice with apparent clinical symptoms significantly reduces the pathological manifestations, namely apoptotic cell death, NFL leakage, histological tissue damage, and glutamate excess, thus corroborating the neuroprotective consequences of this treatment. Full article
(This article belongs to the Special Issue Recent Progress in Multiple Sclerosis)
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16 pages, 10122 KiB  
Article
Myelin Quantification in White Matter Pathology of Progressive Multiple Sclerosis Post-Mortem Brain Samples: A New Approach for Quantifying Remyelination
by Marije J. D. Huitema, Eva M. M. Strijbis, Antonio Luchicchi, John G. J. M. Bol, Jason R. Plemel, Jeroen J. G. Geurts and Geert J. Schenk
Int. J. Mol. Sci. 2021, 22(23), 12634; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms222312634 - 23 Nov 2021
Cited by 4 | Viewed by 2516
Abstract
Multiple sclerosis (MS) is a demyelinating and neurodegenerative disease of the central nervous system (CNS). Repair through remyelination can be extensive, but quantification of remyelination remains challenging. To date, no method for standardized digital quantification of remyelination of MS lesions exists. This methodological [...] Read more.
Multiple sclerosis (MS) is a demyelinating and neurodegenerative disease of the central nervous system (CNS). Repair through remyelination can be extensive, but quantification of remyelination remains challenging. To date, no method for standardized digital quantification of remyelination of MS lesions exists. This methodological study aims to present and validate a novel standardized method for myelin quantification in progressive MS brains to study myelin content more precisely. Fifty-five MS lesions in 32 tissue blocks from 14 progressive MS cases and five tissue blocks from 5 non-neurological controls were sampled. MS lesions were selected by macroscopic investigation of WM by standard histopathological methods. Tissue sections were stained for myelin with luxol fast blue (LFB) and histological assessment of de- or remyelination was performed by light microscopy. The myelin quantity was estimated with a novel myelin quantification method (MQM) in ImageJ. Three independent raters applied the MQM and the inter-rater reliability was calculated. We extended the method to diffusely appearing white matter (DAWM) and encephalitis to test potential wider applicability of the method. Inter-rater agreement was excellent (ICC = 0.96) and there was a high reliability with a lower- and upper limit of agreement up to −5.93% to 18.43% variation in myelin quantity. This study builds on the established concepts of histopathological semi-quantitative assessment of myelin and adds a novel, reliable and accurate quantitative measurement tool for the assessment of myelination in human post-mortem samples. Full article
(This article belongs to the Special Issue Recent Progress in Multiple Sclerosis)
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Review

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27 pages, 692 KiB  
Review
Current and Future Biomarkers in Multiple Sclerosis
by Jennifer Yang, Maysa Hamade, Qi Wu, Qin Wang, Robert Axtell, Shailendra Giri and Yang Mao-Draayer
Int. J. Mol. Sci. 2022, 23(11), 5877; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23115877 - 24 May 2022
Cited by 33 | Viewed by 6082
Abstract
Multiple sclerosis (MS) is a debilitating autoimmune disorder. Currently, there is a lack of effective treatment for the progressive form of MS, partly due to insensitive readout for neurodegeneration. The recent development of sensitive assays for neurofilament light chain (NfL) has made it [...] Read more.
Multiple sclerosis (MS) is a debilitating autoimmune disorder. Currently, there is a lack of effective treatment for the progressive form of MS, partly due to insensitive readout for neurodegeneration. The recent development of sensitive assays for neurofilament light chain (NfL) has made it a potential new biomarker in predicting MS disease activity and progression, providing an additional readout in clinical trials. However, NfL is elevated in other neurodegenerative disorders besides MS, and, furthermore, it is also confounded by age, body mass index (BMI), and blood volume. Additionally, there is considerable overlap in the range of serum NfL (sNfL) levels compared to healthy controls. These confounders demonstrate the limitations of using solely NfL as a marker to monitor disease activity in MS patients. Other blood and cerebrospinal fluid (CSF) biomarkers of axonal damage, neuronal damage, glial dysfunction, demyelination, and inflammation have been studied as actionable biomarkers for MS and have provided insight into the pathology underlying the disease process of MS. However, these other biomarkers may be plagued with similar issues as NfL. Using biomarkers of a bioinformatic approach that includes cellular studies, micro-RNAs (miRNAs), extracellular vesicles (EVs), metabolomics, metabolites and the microbiome may prove to be useful in developing a more comprehensive panel that addresses the limitations of using a single biomarker. Therefore, more research with recent technological and statistical approaches is needed to identify novel and useful diagnostic and prognostic biomarker tools in MS. Full article
(This article belongs to the Special Issue Recent Progress in Multiple Sclerosis)
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17 pages, 337 KiB  
Review
The Role of Molecular Imaging as a Marker of Remyelination and Repair in Multiple Sclerosis
by Ido Ben-Shalom, Arnon Karni and Hadar Kolb
Int. J. Mol. Sci. 2022, 23(1), 474; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23010474 - 31 Dec 2021
Cited by 2 | Viewed by 2408
Abstract
The appearance of new disease-modifying therapies in multiple sclerosis (MS) has revolutionized our ability to fight inflammatory relapses and has immensely improved patients’ quality of life. Although remarkable, this achievement has not carried over into reducing long-term disability. In MS, clinical disability progression [...] Read more.
The appearance of new disease-modifying therapies in multiple sclerosis (MS) has revolutionized our ability to fight inflammatory relapses and has immensely improved patients’ quality of life. Although remarkable, this achievement has not carried over into reducing long-term disability. In MS, clinical disability progression can continue relentlessly irrespective of acute inflammation. This “silent” disease progression is the main contributor to long-term clinical disability in MS and results from chronic inflammation, neurodegeneration, and repair failure. Investigating silent disease progression and its underlying mechanisms is a challenge. Standard MRI excels in depicting acute inflammation but lacks the pathophysiological lens required for a more targeted exploration of molecular-based processes. Novel modalities that utilize nuclear magnetic resonance’s ability to display in vivo information on imaging look to bridge this gap. Displaying the CNS through a molecular prism is becoming an undeniable reality. This review will focus on “molecular imaging biomarkers” of disease progression, modalities that can harmoniously depict anatomy and pathophysiology, making them attractive candidates to become the first valid biomarkers of neuroprotection and remyelination. Full article
(This article belongs to the Special Issue Recent Progress in Multiple Sclerosis)
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